Cigarette smoking remains the number one preventable cause of death and disability in the United States. Over the thousands of cigarettes smoked by a smoker each year, environmental drug cues such as the sight of a pack of cigarettes or another smoker become tightly linked to smoking behavior and the delivery of nicotine to the brain. While it is thought that these associations play an important role in both the maintenance of smoking behavior and relapse to smoking during quit attempts, little is known about the neurobiological basis of these associations, how they are mediated in the brain by drug states such as withdrawal, or what role they play in the subjective experience of drug craving. Thus, the purpose of the present study is to investigate how various drug states alter brain responses to visual smoking cues. Tobacco dependent smokers will receive brain scans on two separate occasions: 1) after overnight deprivation from smoking (deprived condition) and 2) after smoking their usual number and brand of cigarettes (satiated condition). Regional cerebral blood flow as measured by fMRI will be recorded while participants view pictures of smoking cues (e.g., a lit cigarette) and control cues (e.g., car keys). We hypothesize that exposure to smoking and control cues while satiated will result in similar patterns of fMRI signal characterized by increased signal in areas associated with sensory information relay (e.g., thalamus), attention (e.g., anterior cingulate cortex), and visual information processing (e.g., intraparietal sulcus, fusiform gyrus). During smoking deprivation, exposure to smoking cues in comparison to neutral, control cues will result in increased brain signal in regions associated with attention (e.g., anterior cingulate cortex), motivated approach (e.g., left prefrontal cortex), and drug reward (e.g., amygdala, nucleus accumbens, and ventral tegmental area). The relationship between subjective reports of craving for cigarettes and regional brain activation in response to smoking cues will be examined. The results of this study will enhance our understanding of the neurobiological basis of tobacco dependence, inform treatment development, and generate additional hypotheses and research plans.